人类原发性高血压的成因虽经长期研究,尚无结论。多数报道提出人类高血压病与食盐的关系,一般认为高血压患者明显受到食盐摄取量及血钠平衡的影响。然而,食盐的摄取如何引起高血压这一根本问题还未解决。 Dahl制作的对食盐敏感鼠(简称S鼠)和对食盐耐受鼠(简称R鼠)是研究高血压病与食盐关系有用的动物模型。S鼠在低盐时维持正常血压,但高盐则发生高血压。R鼠受食盐摄入量的影响常不明显,且能维持血压正常,说明对食盐的敏感性有个体差异,并同遗传因素有关。实验发现:低盐摄入且血压正常之S鼠的肾内压和钠利尿曲线右移,排泄一定量的钠所需灌流压要比R鼠高。正常血压S鼠的肾髓质乳头 The cause of human essential hypertension despite long-term studies, no conclusion. Most reports raised the relationship between human hypertension and salt, hypertension is generally considered significantly affected by salt intake and serum sodium balance. However, the fundamental problem of how salt intake causes hypertension is unsolved. Salt sensitized mice (S rats) and salt tolerant mice (R rats) made by Dahl are useful animal models for studying the relationship between hypertension and salt. S rats maintain normal blood pressure in low salt, but high salt is hypertension. R rats affected by salt intake is often not obvious, and can maintain normal blood pressure, indicating the individual differences in salt sensitivity, and with genetic factors. Experiments found that: low salt intake and normal blood pressure in rats with renal S pressure and sodium diuretic curve to the right, excretion of a certain amount of sodium required perfusion pressure than R rats higher. Normal rat S renal medulla nipple